Indirect vascular actions of (Gln4)-neurotensin in canine adipose tissue.

The vasoconstrictor action of the tridecapeptide (Gln4)-neurotensin has been studied in subcutaneous adipose tissue in the inquinal region of anesthetized dogs. Close intra-arterial infusion of (Gln4)-neurotensin, 30--120 pmol X kg-1 b.wt. X min-1, elicited similar vasoconstrictions in the adipose tissue on the infusion side and on the contralateral side. This suggests that (Gln4)-neurotensin must enter the general circulation before it can elicit vasoconstriction. Removal of parts of the gastrointestinal tract did not change the vasoconstrictor response. Thus, there is no indication of release of vasoactive substances from the gastrointestinal tract by (Gln4)-neurotensin. Infusion into the portal vein elicited the same vasoconstriction in adipose tissue as the same dose administered i.v. It is suggested that the vasoconstrictor action in adipose tissue is not caused by (Gln4)-neurotensin per se. Instead, vasoactive substance(s) may be formed from (Gln4)-neurotensin.